Summary

14-3-3 proteins have been extensively studied from yeast to mammals and associated with multiple roles ranging from fundamental processes such as cell cycle, apoptosis and stress response to diseases such as cancer. In Caenorhabditis elegans, there are two 14-3-3 genes, ftt-2 and par-5. The ftt-2 gene is expressed only in somatic lineages, whereas par-5 expression is detected in both soma and germline. In early embryonic development, par-5 is necessary to establish cell polarity. Although it is known that par-5 inactivation results in sterility, the role of this gene in germline development is poorly characterized. In the present study, we use a par-5 mutation and RNA interference to characterize par-5 functions in the germline. The lack of par-5 in germ cells causes cell cycle deregulation, the accumulation of endogenous DNA damage and genomic instability. Moreover, par-5 is required for checkpoint-induced cell cycle arrest in response to DNA-damaging agents. We propose a model where PAR-5 regulates CDK-1 phosphorylation to prevent premature mitotic entry. This study opens a new path to investigate the mechanisms of 14-3-3 functions, which are not only essential for worm development but also have been shown altered in human diseases.

Marian Blanca Ramírez from the CSIC in Spain has been studying the effects of LRRK2, a protein associated with Parkinson’s disease, on cell motility. A Travelling Fellowship from Journal of Cell Science allowed her to spend time in Prof Maddy Parson’s lab at King’s College London, learning new cell migration assays and analysing fibroblasts cultured from individuals with Parkinson’s. Read more on her story here.

Where could your research take you? The deadline to apply for the current round of Travelling Fellowships is 23rd Feburary 2018. Apply now!